Practicals Term I (+BP Prac) Flashcards

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1
Q

Gram +ve bacteria

A
  • have thick peptidoglycan cell walls
  • stain purple/blue
  • like dry environments
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2
Q

Gram +ve cocci on Gram stain suggest

A

normal flora

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3
Q

Gram -ve bacteria

A
  • have thin peptidoglycan cell walls and an outer membrane
  • do not stain (ie pink or red)
  • like moist environments
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4
Q

Gram +ve clusters are

A

Staphylococci

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5
Q

Gram +ve chains are

A

Streptococci

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6
Q

Green pus is likely caused by

A

Pseudomonas aeruginosa

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7
Q

Sulphur granules in pus indicate

A

Actinomyces israelii

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8
Q

Pus with an offensive odour is likely caused by

A

anaerobes

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9
Q

Thick, yellow pus is likely caused by

A

Staphylococcus aureus, etc.

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10
Q

Genetics account for what percent of BP variation in the population?

A

40%

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11
Q

What happens to systolic BP on sitting??

A

drops slightly; then restored (but not to lying pressure)

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12
Q

What happens to SV on sitting from lying?

A
  • decreases
  • perceived as a slight drop in BP by baroreceptors in carotids and aorta as decreased stretch
  • baroreceptors fire to activate medulla to increase SNS tone and decreased PNS tone
    • increased SNS and decreased PS increase HR and contractility to restore SV(but not to same level as lying)
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13
Q

What happens to systolic BP on standing from sitting?

A

initial drop in BP; restored

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14
Q

What happens to SV on standing from sitting?

A

drops; activates +SNS and -PNS via baroreceptor reflex to increase HR and restore SV

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15
Q

What happens to HR from lying to standing?

A

increases

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16
Q

What happens to diastolic BP from lying to standing?

A

decreases

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17
Q

What happens to cardiac output from lying to standing?

A

decreases

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18
Q

What happens to total peripheral resistance from lying to standing?

A

decreases

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19
Q

How does the body increase MAP from lying to standing?

A

by increasing TPR

(inc HR would compromise diastolic filling of coronaries)

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20
Q

Nicotine

A

increases BP, HR

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21
Q

Caffiene

A

initially increases blood pressure, long-term effects unknown

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22
Q

What are primary immunodeficiencies?

A
  • result of inherent congenital defects in the components of the immune system or their products
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23
Q

What are secondary immunodeficiencies?

A
  • result from effects of external agents or alterations in other body systems
  • more common than primary
  • associated with:
    • extremes of age
    • malnutrition
    • anatomic barrier dysfunction (incl medical devices)
    • non-infectious diseases (diabetes, tumours/cancer)
    • infections (malaria, HIV)
    • cytotoxic drugs/irradiation (chemo)
    • immunosuppresive drugs
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24
Q

Secondary immunodeficiencies are associated with

A
  • extremes of age
  • malnutrition
  • anatomic barrier dysfunction (incl medical devices)
  • non-infectious diseases (diabetes, tumours/cancer)
  • infections (malaria, HIV)
  • cytotoxic drugs/irradiation (chemo)
  • immunosuppresive drugs
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25
Q

Recessive gene defects that cause primary immunodeficiencies include

A
  • defects in development of primary lymphoid tissue (thymus, spleen)
  • defects in T cell development
  • MHC Class I or II deficiency
  • defects in B cell development and selected antibody deficiencies
  • phagocyte deficiencies
  • complement pathway deficiencies
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26
Q

What blood specimens are collected for immunodeficiency diagnosis?

A
  • blood - anticoagulant:
    • # s and function of immune cells
  • blood - plain tube:
    • clots; for complement and antibody estimations
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27
Q

What is the order of isotype switching?

A

IgM > IgG > IgE > IgA

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28
Q

How is blood analysed for populations of lymphocytes?

A

flow cytometry using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies as markers

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29
Q

How are lymphocytes analysed in the blood?

A
  • flow cytometry for populations using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies
  • antibody isotype analysis (IgG, IgM, IgE, IgA)
  • specific antibody analysis (tetanus, blood groups)
  • t-cell proliferation tests
  • flow cytometry of CD40L expression on activated lymphocytes
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30
Q

How is B-cell function analysed?

A

presence of antibodies made against immunisation antigens and blood group antigens

31
Q

If B cell populations are normal but isotype switching is not occurring, where is the immunodeficiency?

A

T-cells; required for isotype switching

32
Q

How is T-cell function analysed?

A
  • inducing T-cell proliferation by reacting them with anti-T/anti-CD3 antibodies
    • proliferation requires CD25 receptor for IL-2
  • expression of CD40L using flow cytometry on activated T cells
33
Q

CD40L is on

A

T-cells

34
Q

What is the function of CD40L?

A
  • required for activating B-cells
    • CD40L on T-cells binds to CD40 on B-cells to activate them
  • necessary for isotype switching of B cells
    • deficiency can cause hyper IgM (isotype cannot switch to IgG)
  • activates macrophages
    • deficiency means lack of inflammatory cytokine production (afebrile in infection), and defective respiratory burst
  • deficiency can also result in:
    • poor memory B cell production
    • inefficient induction of cyotoxic T-cells
35
Q

The gene for CD40L is on which chromosome?

A

X; tf deficiency is x-linked

36
Q

What is affinity maturation?

A

the process by which B cells produce antibodies with increased affinity for antigen during the course of an immune response

37
Q

Monocyte function can be analysed by

A
  • assessing production of TNFa in response to stimulation by IFNy
    • TFNa stimulates granuloma formation, macrophage differentiation into giant cells etc.
    • tf deficiency in IFNy or IFNyR1 on macrophages results in decreased TNFa production and no granuloma formation where there should be (eg mycobacterium infections)
  • flow cytometric analysis for the expression of IFNyR1 (receptor) on monocytes
38
Q

IFNy is produced by

A

activated CD4 T cells (particularly Th1)

CD8 T-cells

NK cells

39
Q

IFNy activates

A

macrophages

40
Q

What organisms are common in complicated UTI?

A
  • proteus
  • klebsiella
  • enterococci
  • pseudomonas
41
Q

Complicated UTIs are associated with

A
  • anatomical abnormalities (including medical devices)
  • metabolic abnormalities (pregnancy, diabetes)
  • immunocompromise
  • unusual pathogens (yeasts)
42
Q

What bacteria cause UTIs?

A
  • E coli (70-95%)
  • Staph saprophyticus (10-20% in sexually active females)
  • Proteus (GIT flora)
  • Klebsiella (GIT flora)
  • Enterococci (GIT flora)
  • Pseudomonas (environmental)
43
Q

What laboratory investigations are undertaken for suspected UTI?

A
  • dip-stick for RBCs, leukocyte exterase, nitrites, protein
  • pyuria (pus) measured by counting WBC; >10^4-10^5/mL is abnormal
  • casts and crystals (microscopy)
  • culture; >10^8/L (>10^5/mL) organisms of a single type in MSU is significant, any grwoth from SPA is significant
44
Q

What is an abnormal WBC count in urinalysis?

A

>10^4-10^5/mL

45
Q

What culture count is significant in UTI?

A

>10^8/L (>10^5/mL)

46
Q

What count of RBCs in urine is abnormal?

A

>2000/mL

47
Q

Presence of RBC casts on urinalysis indicates

A

bleeding in the kidney

48
Q

What media are used in urinalysis?

A
  • HBA (aerobic)
  • MAC (aerobic)
  • CLED (aerobic)
  • Lowenstein-Jensen if renal TB suspected
  • Selenite broth if suspected Salmonella Typhi carrier
49
Q

Bactaeremia

A
  • bacteria in blood
  • transient (not uncommon), intermittent, or continuous
  • not necessarily associated with clinical features
  • requires a mode of entry
50
Q

Septicaemia

A
  • bacteraemia causing symptoms
    • fever, increased CO and RR, changes to body systems/perfusion of organs
  • serious
  • systemic - sepsis or septic shock
51
Q

Sepsis

A
  • septicaemia infection
  • fever or hypothermia
  • tachypnoea or tachycardia
  • high or low white cell counts
52
Q

Septic shock

A
  • severe sepsis
  • potentially fatal drop in BP
53
Q

Bacteria and septicaemia result from

A
  • infection
  • massive traua
  • inflammatory disease
54
Q

Systemic inflammatory response syndrome

A

two or more of:

  • temperature >38C or <36C
  • resp rate >20/min
  • HR >90/min
  • WBC >12x10^9/L or <4x10^9/L or >10% immature cells
55
Q

What are the common gram positive causes of septicaemia?

A
  • staph aureus
  • strep pyogenes
  • staph epidermidis
  • viridans strep
  • strep pneumoniae
  • enterococcus spp
56
Q

What are common gram negative causes of septicaemia?

A
  • E. coli
  • pseudomonas aurigenosa (environmental)
  • klebsiella
  • enterobacter spp
  • nisseria meningitidis
57
Q

What are other common causes of septicaemia?

A
  • Candida
  • rickettsiae
58
Q

What are some of the risk factors for septicaemia?

A
  • impaired immunity
    • breached integument, neutropenia
  • hospitalization
  • indwelling (bladder) catheterization
  • overseas travel
  • occupational
  • contact with animals, contaminated food, water
  • infection by a virulent pathogen
59
Q

Sources of septicaemia bacteria are

A
  • skin
  • URT
  • genito-urinary tract
  • GI/biliary tract
60
Q

GPC are either

A

staph or strep

61
Q

Staph is catalase

A

+ve

62
Q

Strep is catalase

A

negative

(as is enterococci)

63
Q

Staph aureus is coagulase

A

+ve

64
Q

Coagulase negative staph are likely

A

epidermidis (susceptible to novobiocin)

saprophyticius (resisitant to novobiocin)

65
Q

URTIs are commonly caused by

A

viruses

66
Q

sore throat is predominaly

A

viral infection

67
Q

sinusitis is predominantly

A

bacterial infection (often post-viral)

68
Q

otitis media is often

A

bacterial infection

69
Q

LRTIs include

A
  • croup (laryngotracheobronchitis)
  • whooping cough
  • bronchiolitis
  • bronchitis (acute and acute exacerbation of chronic)
  • pneumonia
70
Q

What number of microorganisms in sputum suggest infection?

A

>10^7/mL

especially of one type

71
Q

Small numbers of small pink colonies on MAC suggest

A

growth of normal microbiota (eg e. coli)

72
Q

How do conjugate vaccines work?

A
  • polysaccharide of capsule conjugated to protein = antigen
  • protein antigen presented by APCs to T cells activates them to express CD40L
  • polysaccharide antigen recognized by Ig on B cells internalized the conjugate
    • peptide portion presented on MHC class II of B cell
  • activated T cell binds MHC class II peptide on B cell, CD40 on B cell ligates CD40L
  • induces isotype switching, affinity maturation, memory cell secretion
  • polysacch on its own cannot activate T cells; can activate some (CD5) B cells (T-indep) but regardless only get IgM and no secondary immune response
  • tf peptide conjugate is vital to generating isotype switch and secondary immune response
73
Q

What is haemolytic uremic syndrome?

A
  • haemolytic anaemia +
  • acute kidney failure (uremia) +
  • low platelet count (thrombocytopoenia)
74
Q
A